concern for causing dehydration.We started oral administration of FC 0.2 g daily and successfully tapered and stopped hypertonic NaCl.Results: CSWS features pathological volume loss from kidney and the proposed mechanism causing hyponatremia is that volume depletion stimulates physiological AVP secretion, different from SIADH or adrenal insufficiency.In our case, dilation of IVC and raised blood pressure while administrating NaCl could not disprove tendency toward fluid loss, but could prove absent of volume depletion causing AVP secretion.Thus, hypertonic urine suggested the presence of ongoing AVP effect from other stimuli (e.g.brain tumor, stress), in turn contradicting CSWS.His sinuses cancer inhibited nasal breathing and provoked thirst, leading to insufficient water restriction.It is presumed that to treat SIADH (or adrenal insufficiency) inadequate fluid restriction demanded lots of hypertonic NaCl, inducing significant diuresis, may resembling CSWS.Although FC was thought to improve hyponatremia in CSWS via restoration of volume, it should act through different mechanism in our case.Even though adrenal insufficiency was not disproved in our case, taking into account the previous report of efficacy of FC for SIADH at least temporarily and the recent research about effect of mineralocorticoid on AVP secretion, it is necessary to reassess how FC improves hyponatremia.Conclusion: Our case implies the importance of reassessing hyponatremia cases in terms of what triggers and resolves AVP secretion.I have no potential conflict of interest to disclose.I did not use generative AI and AI-assisted technologies in the writing process.
Madan et al. (Wed,) studied this question.